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INIPharma S.A. de C.V.

Inipharm is a biopharmaceutical company developing small-molecule inhibitors targeting the HSD17B13 protein to treat severe liver diseases, including nonalcoholic steatohepatitis (NASH) and fibrosis. Their approach leverages genetic insights that link HSD17B13 variants to reduced liver disease severity, aiming to improve liver health outcomes through anti-fibrotic therapies.

Seattle, United States450+ followers
Updated 2 months ago

Funding

Funding not disclosed

Funding rounds are not available yet.

Founders

Founder details are not available yet.

Product

Problem

Severe liver diseases, such as nonalcoholic steatohepatitis (NASH) and fibrosis, lack effective treatments, leading to significant morbidity and mortality. Current therapeutic options often fail to address the underlying genetic factors contributing to disease progression. There is a need for targeted therapies that can effectively inhibit key proteins involved in liver disease pathogenesis.

Solution

Inipharm is developing small-molecule inhibitors targeting the HSD17B13 protein to treat severe liver diseases, including NASH and fibrosis. The company's approach is based on genetic evidence linking variants in HSD17B13 expression to reduced liver disease severity. Inipharm's inhibitors have demonstrated anti-fibrotic effects in human liver cell-based systems and improved liver enzymes in in vivo models. Their lead development candidate, INI-822, replicates lipidomic changes seen with protective HSD17B13 variants. By targeting HSD17B13, Inipharm aims to improve liver health outcomes through anti-fibrotic therapies.

Target Audience

The primary target audience includes patients with severe liver diseases such as nonalcoholic steatohepatitis (NASH) and fibrosis, as well as hepatologists and other physicians treating these conditions.

Features

  • Small-molecule inhibitors of HSD17B13
  • INI-822 development candidate
  • Demonstrated reduction of fibrotic markers in human liver cell models
  • Improved liver enzyme profiles in multiple in vivo models
  • Replicated lipidomic changes associated with protective HSD17B13 variants
  • Targets pathways associated with lipotoxicity, inflammation, and fibrosis
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